CMR Cine-based Hemodynamic Forces Analysis for Detection of Constrictive Physiology in Pericarditis

Background: Constrictive physiology can accompany both acute and chronic pericarditis. Its recognition is clinically important because it guides therapy, yet it remains diagnostically challenging, underscoring the need for reliable quantitative markers. Hemodynamic forces (HDF) analysis is a novel noninvasive approach that interrogates intraventricular blood-flow dynamics and reflects global intraventricular pressure gradients (IVPGs). This study aimed to determine whether cine-derived feature-tracking strain and hemodynamic force (HDF) metrics from routine cine CMR can discriminate pericarditis with constrictive physiology (CP) from non-constrictive pericarditis (NCP).

Methods: In this retrospective study, patients with clinical and CMR-confirmed diagnosis of pericarditis (from 2010 to 2024) were screened and patients with evaluable strain and HDF analysis without concomitant cardiac disease were included. Patients were divided into an NCP and a CP group. The latter was defined as a composite of clinical, transthoracic echocardiography (TTE) and CMR-based diagnosis of constrictive physiology including ventricular septal shift with respiration following Majo criteria. Besides standard left ventricular (LV) CMR analysis, LV strain parameters (global longitudinal [GLS] and circumferential strain [GCS]) and HDF parameters (e.g., strength apical-basal and septal-lateral) were assessed (QMass and HDF, Medical Imaging Systems). Student’s t-test, univariable analysis and receiver operating characteristic (ROC) analysis were performed.

Results: A total of 103 patients with pericarditis (mean age, 53±18 years; 66 men [64%]) were included. Nearly half of the cohort presented with acute chest pain (44/103; 48%). The most common etiologies were idiopathic (46%), autoimmune (26%), and infectious (18%). 61/103 (59%) were classifies as NCP, and 42/102 (41%) had constrictive physiology (CP group). There was no significant difference between the NCP and the CP group in LV ejection faction (59±8% vs 60±7%, p=0.17), but in LV end-diastolic volume index (75±18ml/m² vs 62±17ml/m², p=0.003). Compared to the NCP group, myocardial strain and HDF parameters were impaired in the CP group (GLS: -22.2±3.9 vs -18.11±4.6, p< 0.001; GCS: -31.9±5.4 vs -27.2±6.8, p< 0.001; HDF apex-base strength: 21.4±7.3% vs 15.3±6.2%, p< 0.001; HDF impulse: 23.9±8.3% vs 16.4±7.4%, p< 0.001). HDF apex-base and GLS were associated with presence of constrictive physiology (OR 0.83 [0.73-0.93], p=0.002 and OR 1.21 [1.05-1.40], p=0.007) on multivariable analysis. HDF apex-base and GLS achieved the highest diagnostic performance for dectection of constrictive physiology (AUC 0.78 [0.69-0.88] and AUC 0.76 [0.67-0.86]).

Conclusion: CMR cine-based strain and hemodynamic force analysis can be used for quantitative detection of constrictive physiology in pericarditis.

Tabel 1: Characteristics of study population with non-constrictive and constrictive pericarditis

	All patients n = 103	Non-constrictive pericarditis n = 61	Constrictive pericarditis n = 42	p-Value
Age (y)	52.7±18.4	50.4±18.1	56.1±18.4	0.130
Male sex (n)	66 (64)	35 (57)	31 (74)	0.099
Body mass index (kg/m2)	25.9±4.9	25.2±5.3	26.8±3.9	0.116
Body surface area (ml/m2	1.9±0.3	1.9±0.3	2.0±0.2	0.336
Symptom onset to CMR (d)	21.2±39.3	27.2±49.8	13.2±13.6	0.098
Acute chest pain (n)	44 (48)	28 (53)	16 (42)	0.396
ECG abnormalities (n)	37 (45)	21 (41)	16 (50)	0.499
Etiology
Infectious (n)	19 (18)	9 (15)	10 (24)
Autoimmune (n)	27 (26)	17 (28)	10 (24)
Neoplastic (n)	2 (2)	2 (3)	0 (0)
Traumatic and Iatrogenic (n)	8 (8)	5 (8)	3 (7)
Idiopathic (n)	47 (46)	28 (46)	19 (45)
Laboratory testing
Trop T (ng/l)	31.7±46.7	37.5±55.9	21.9±20.1	0.243
NT pro-BNP (pg/ml)	1722.5±4023.0	1299.6±1960.4	2303.9±5707.1	0.461
C-reactive proteine (mg/l)	84.5±77.4	77.9±69.2	93.5±86.6	0.369
Leucocytes (103/μml)	10.9±4.3	10.9±4.0	10.9±4.7	0.988
Hematocrit (%)	35.7±6.0	35.1±6.4	36.6±5.2	0.056

Table 2: CMR characteristics of study population with non-constrictive and constrictive pericarditis

	Non-constrictive pericarditis n = 61	Constrictive pericarditis n = 42	p-Value
Morphology and function
Heart rate (min-1)	77±19	75±12	0.678
LV ejection fraction (%)	58.6±7.9	59.5±6.9	0.173
LV end-diastolic volume (ml)	147.9±43.6	124.5±38.7	0.035
LV end-diastolic volume index (ml/m2)	75.4±18.2	62.0±16.7	0.003
Interventricular septal thickness at diastole (mm)	9.3±2.2	9.0±1.5	0.343
Pericardial effusion (n)	47 (77)	28 (67)	0.267
Thickness (mm)	14.2±9.8	13.7±9.3	0.115
Aortic valve (mm)	22.8±2.9	23.5±2.6	0.225
Mitral valve (mm)	34.1±3.7	35.3±5.1	0.175
Tissue characterization
Pericardial edema (n)	51 (84)	33 (79)	0.608
Segmental (n)	10 (20)	4 (12)	0.550
Global (n)	41 (80)	29 (88)	0.550
Pericardial LGE (n)	61 (100)	41 (98)	0.408
Segmental (n)	16 (26)	4 (10)	0.045
Global (n)	45 (74)	37 (90)	0.045
Myocarditis-pattern LGE (n)	8 (13)	4 (10)	0.757
Left ventricular myocardial strain
Global longitudinal strain (%)	-22.2±3.9	-18.11±4.6	< 0.001
Global circumferential strain (%)	-31.9±5.4	-27.2±6.8	< 0.001
Hemodynamic forces (HDF)
Entire heart beat HDF strength (RMS)
A-B (%)	21.4 ± 7.3	15.3 ± 6.2	< 0.001
L-S (%)	4.9 ± 2.7	4.2 ± 1.5	0.145
L-S/A-B ratio	23.1 ± 9.2	29.6 ± 10.4	0.001
HDF force angle φ	72.4 ± 4.9	69.7 ± 5.1	0.008
Systolic impulse (%)	23.9 ± 8.3	16.4 ± 7.4	< 0.001
Systolic peak (%)	49.3 ± 19.3	33.7 ± 15.0	< 0.001

Figure shows a representative CMR example of a patient with acute pericarditis and with constrictive physiology including HDF analysis.